Glucosamine Inhibits Lipopolysaccharide-induced Inflammatory Responses in Human Periodontal Ligament Fibroblasts.
10.11620/IJOB.2014.39.4.221
- Author:
Eun Dam KIM
1
;
Hyun Jung PARK
;
Jeong Hwa BAEK
Author Information
1. Department of Molecular Genetics, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 110-749, Korea. baekjh@snu.ac.kr
- Publication Type:Original Article
- Keywords:
human periodontal ligament fibroblasts;
glucosamine;
lipopolysaccharide;
inflammation;
NF-kappaB
- MeSH:
Aged;
Animals;
Blood Vessels;
DNA;
Enzyme-Linked Immunosorbent Assay;
Fibroblasts*;
Glucosamine*;
Heart;
Humans;
Inflammation;
Interleukin-6;
Interleukin-8;
NF-kappa B;
Osteoarthritis;
Periodontal Ligament*;
Periodontitis;
Phosphotransferases;
Prescriptions;
RNA, Messenger
- From:International Journal of Oral Biology
2014;39(4):221-228
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Glucosamine is commonly taken by the elderly without prescription as a nutritional supplement to attenuate the progression or symptoms of osteoarthritis. Previous studies demonstrated that glucosamine shows anti-inflammatory effects in tissues such as blood vessels and the heart. However, there have been few reports about the effects of glucosamine on oral inflammatory diseases. Therefore, in this study, the effects of glucosamine on lipopolysaccharide (LPS)-induced inflammatory responses were investigated using human periodontal ligament fibroblasts (HPDLFs). HPDLFs were incubated in the presence and absence of glucosamine (10 mM) for 24 h, followed by treatment with E. coli LPS (100 ng/ml) or vehicle. Quantitative RT-PCR and ELISA results showed that LPS exposure significantly increased the levels of IL-6 and IL-8 mRNA and protein, while the effect was significantly suppressed by glucosamine treatment. Glucosamine did not attenuate, but slightly increased, the LPS-induced activation of mitogen activated kinases (ERK, p38, JNK). However, it suppressed the LPS-induced increase in the DNA binding affinity and transcriptional activity of NF-kappaB. These results suggest that glucosamine exerts anti-inflammatory effects on HPDLFs exposed to LPS via inhibition of NF-kappaB activity, necessitating further studies using animal periodontitis models.
